Skip to main content
. 2021 Feb 25;11:605025. doi: 10.3389/fonc.2021.605025

Figure 2.

Figure 2

FOXP2 inhibited the EMT of breast cancer cells. (A) The changes of the morphology at day 6 post epidermal growth factor (EGF) treatment (100 ng/ml) in MCF-7 cells were pictured by TE2000S (Nikon, 200×). (B, C) The expression of FOXP2 was downregulated during EGF-induced epithelial-mesenchymal transition (EMT) in MCF-7 cells. MCF-7 cells were treated with EGF (100 ng/ml) and harvested at different time points (day 0, day 3, day 6) post the treatment. The levels of FOXP2, E-cadherin, and Vimentin were examined by Western blotting (B) and qPCR (C), respectively. (D–F) Knockdown of FOXP2 enhanced EMT in MCF-7 cells. MCF-7 cells were infected with one of lentiviral vectors expressing various FOXP2-specific shRNA (Lv-shFOXP2#1, #2, #3) or the control lentiviral vector (Lv-shCon). The stable FOXP2-knockdown MCF-7 cells were selected and harvested for protein and total RNA preparation. The levels of FOXP2, E-cadherin, and Vimentin were examined by Western blotting (D) and qPCR (E). The migration ability of Lv-shCon-infected MCF-7 cells (shCon) and Lv-shFOXP2#2-infected cells (shFOXP2) was measured by the Transwell invasion test and the statistical data are shown on the right (F). (G–I) Overexpression of FOXP2 abolished the mesenchymal phenotype of MDA-MB-231 cells. MDA-MB-231 cells were transfected with pHis-FOXP2 or the control vector pCMV-EGFP. The levels of FOXP2, E-cadherin, and Vimentin were examined by Western blotting (G) and qPCR (H). The migration ability of control vector transfected MDA-MB-231 cells (231) and FOXP2-expressing MDA-MB-231 cells (FOXP2) was measured by the Transwell invasion test and the statistical data are shown on the right (I). The asterisks indicate statistically significant changes: *P ≤ 0.05, **P ≤ 0.01, and ***P ≤ 0.001.